Background Helicobacter pylori eradication with therapies employing a proton pump inhibitor (PPI) and antimicrobial agents is mainly achieved via bacterial susceptibility to antimicrobial agents and the magnitude of acid secretion inhibition. However, annual eradication rates have greatly declined in Mainland China, and therefore, tailored H. pylori eradication regimens that inhibit acid secretion and employ optimal antimicrobial agents determined based on gene clip testing may improve eradication rates. This study was aimed at evaluating the efficacy of tailored H. pylori eradication therapy guided by visual gene clip testing for antibiotic resistance and PPI metabolism genotypes. Methods This prospective study included 244 patients (141 men and 103 women aged 20–79 years) receiving initial treatment for H. pylori infection. Visual gene clip testing using gastric mucosal specimens was performed to detect antibiotic resistance to clarithromycin conferred by the A2142G and A2143G point mutations of the H. pylori 23S rRNA gene and to levofloxacin conferred by the Asn87 and Asp91 point mutations of the H. pylori gyrA gene. Patients received a 14-day bismuth quadruple therapy regimen guided by testing for antibiotic resistance and CYP2C19 polymorphisms, and primary H. pylori eradication was assessed at least 4 weeks after therapy. Results H. pylori strains were successfully isolated from the gastric mucosa tissues of 244 patients. Antibiotic resistant isolates were identified in 63 patients, with clarithromycin resistance observed in 50 patients, levofloxacin resistance in 7 patients, and dual resistance in 6 patients. The PPI metabolic genotype of CYP2C19 was detected in 242 of 244 cases, and 97 cases were categorized as extensive metabolizers, 141 as intermediate metabolizers, and 4 as poor metabolizers. Among the 242 patients who received tailored therapy, the H. pylori eradication rate was 90.9% (95% confidence interval 87.3%~94.6%) in the intention-to-treat analysis and 96.9% (95% confidence interval 94.7%~99.2%) in the per protocol analysis. Conclusions Tailored therapy for H. pylori infection guided by determination of antibiotic resistance and CYP2C19 polymorphism using visual gene chip technology may provide high clinical effectiveness as initial H. pylori eradication therapy.

Aim: To explore the role of miR-196a on the regulatory mechanism in hepatocelluar carcinoma.Methods: The antisense RNA of microRNA-196a was synthesized and cloned into the vector. HepG2 cells were infected by inhibiting miR196a vector. The HepG2 cells were divided into miR196a lower expression group, NC group and N group in vitro. The expression of the targets of miR-196a was detected by qPCR. Cell growth was analyzed by cck8 assay. The invasion was detected by transwell method. Apoptosis was detected by annexinV/PI. The P53, caspase-3, HOXB9, HOXB8 mRNA and their protein was detected by qPCR and Western-blot.Results: (1) The expression level of miR-196a was less than normal (41%). (2) The proliferation of HepG2 was also markedly suppressed in inhibiting miR196a at the 24 h point than normal about 72.29 +/- 2.51% (P < 0.01). (3) The number of cells that migrated through the chamber of miR196a inhibiting group is less than normal and NC (P < 0.01). (4) The cell apoptosis in miR196a inhibiting group is more than NC and normal group (P < 0.05). HOXB8 mRNA and protein expression, in HepG2 cell line miR196a inhibiting group is significantly less than normal, NC (P < 0.05). Caspase-3 mRNA and protein expression is maximum in three groups (P < 0.05). In three groups there was no significant difference in the expression of P53 mRNA and protein and HOXB9mRNA.Conclusions: Our results demonstrate that miR-196a can effect the proliferation, the apoptosis and migration of HepG2 cell lines by gene HOXB8, caspase-3 regulation. However, there is no correlation between miRNA196a and P53 and HOXB9. (C) 2015 Elsevier Masson SAS. All rights reserved.

OBJECTIVE To test the expression of AQP8 in ascending and descending colon mucosa of diarrhea-irritable bowel syndrome (D-IBS) patients and to study the relationship between IBS and AQP8 as well as the pathological mechanism for D-IBS. METHODS The proximal ascending colon and the distal descending colon of 26 D-IBS sufferers were resected. Total RNA was purified from each sample of mucosa and AQP8 mRNA expression was analyzed with fluorescent quantitative RT-PCR. Analysis was conducted with regard to five aspects of the sufferers, i.e. their sex, age at first incidence, duration of illness, frequency of defecation and characteristics of stool. Correlation analysis of the level of AQP8 mRNA expression in the ascending colon and descending colon was made, and relationship between the expression of AQP8 and the incidence and clinical features of D-IBS explored. RESULTS AQP8 expression was present in specimens of the ascending colon and descending colon of both healthy persons and D-IBS sufferers. Sufferers of D-IBS showed a remarkably lower level of AQP8 expression than the normal controls (Mean 3.1 x 10(4) copies/microg RNA and 2.8 x 10(4) copies/microg RNA vs 8.2 x 10(4) copies/microg RNA and 3.8 x 10(4) copies/microg RNA). The level of AQP8 expression was not correlated with the age of the sufferers or age at first incidence, but was closely correlated with the duration of illness, frequency of defecation and characteristics of stool. The longer the illness lasted, the higher the frequency of defecation and the larger the amount of water was found in stool, the lower the level of AQP8 mRNA expression in colonic mucosa. CONCLUSIONS The decrease in AQP8 expression in sufferers of D-IBS indicates that colonic absorption function is disordered. As a result, absorption of water is reduced, thus loose stool and diarrhoea occur. There may be some correlation between the variation in AQP8 and the incidence of D-IBS.